Gout is a common and complex form of arthritis that can affect anyone. It’s characterized by sudden, severe attacks of pain, swelling, redness and tenderness in the joints, often the joint at the base of the big toe.
An attack of gout can occur suddenly, often waking you up in the middle of the night with the sensation that your big toe is on fire. The affected joint is hot, swollen and so tender that even the weight of the sheet on it may seem intolerable.
Gout symptoms may come and go, but there are ways to manage symptoms and prevent flares.
Uric acid metabolism
Nitrogenous compounds are continuously derived from digestion of proteins in ingested food, degradation of nucleic acids, purine salvage pathways, de novo purine biosynthesis, and purine nucleotide interconversion. Nitrogenous waste products are highly toxic; therefore, efficient mechanisms of elimination have evolved, that are optimally suited for the particular class of organism. All animals excrete three main nitrogenous products – ammonia, urea and uric acid – as well as minor nitrogen excretory products.
Normal Range of Uric Acid in Blood:
2.6-6.0 mg/dl (Female)
3.5-7.2 mg/dl (Male)
Excess accumulation of uric acid in the blood can lead to a disease known as gout. This painful condition is the result of accumulation of needle-like mono sodium urate crystals of uric acid precipitating in joints.
DIET– Normally Prescribed
Mainly Purine Rich Diet is not prescribed.
Inflammation during attacks is more commonly treated with NSAIDs or corticosteroids, and urate levels are managed with allopurinol
Internal Purines, Uric Acid And Gout
- When cells die in our bodies, complex chemical reactions breakdown the cell contents, forming purines and other substances.
- Our bodies produce a substance called Xanthine Oxidase (XO), that turns purines into uric acid
- Our kidneys extract uric acid from blood, then return most of it, excreting any surplus. Several factors will influence what our kidneys consider to be a surplus, and that process can be changed by genetics, the amount of protein in our diet, other substances such as alcohol and some medicines.
- Where uric acid becomes too concentrated in our blood, it will pass into joints and other tissues, where it may form the crystals that cause gout.
It is important to realize from this that, irrespective of diet; our bodies produce their own uric acid supply. Complex processes work on the raw materials (purines), and may create the excess uric acid that can cause gout.
External Purines, Uric Acid And Gout
- External purines from our diet simply increase the raw materials available for uric acid production. If our bodies have problems in parts of the internal purine processing described above, then external purines might make the problem worse, but they do not cause gout directly.
- When uric acid processing problems lead to gout, do not ban all your favorite foods. Life will become miserable, and you might achieve nothing. Yes, reducing external purines has a good chance of reducing uric acid. But it is a slight reduction, which is rarely sufficient to bring uric acid in the blood down to safe levels.
“Think of traffic at a busy intersection. When all is OK, the traffic flows, but if there is an accident, extra traffic adds to delays – it does not (usually) cause more accidents. Traffic is internally generated as an essential part of city life, and it can be increased by external traffic from visitors. When traffic problems occur, we do not ban visitors, though we might advise alternate routes.”
Different types of Purines
Scientists have known for decades that there are different kinds of purines, and that each has a different action when taken as part of our diet. This involves complicated processes that can vary from person to person, so even the best analysis of relevant purine rich foods can only produce an estimate that should be confirmed with uric acid blood tests.
Zollner’s analysis of purine metabolism suggests that xanthine and hypoxanthine are the most effective purines for increasing uric acid. Hence reffered as “Gout Purines” and So restrict the purine rich foods to those compounds.
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•Took the data in this table from Food Composition and Nutrition Tables, 7th revised and completed edition, by Souci, Fachmann, Kraut.
• Values are for 100g. Divide by 100 and multiply by your portion size for your diet analysis.
• Figures are averages of several tests – natural products will vary, and cooking methods can affect final results
The actual evidence, however, has always been less-than-compelling: Just as low cholesterol diets have only a trivial effect on serum cholesterol levels, for instance, and low-salt diets have a clinically insignificant effect on blood pressure, low-purine diets have a negligible effect on uric acid levels.
A nearly vegetarian diet, for instance, is likely to drop serum uric acid levels by 10 to 15% percent compared to a typical American diet, but that’s rarely sufficient to return high uric acid levels to normality, and there is little evidence that such diets reliably reduce the incidence of gouty attacks in those afflicted.
Thus, purine-free diets are no longer prescribed for the treatment of gout, as the gout specialist Irving Fox noted in 1984, “because of their ineffectiveness” and their “minor influence” on uric acid levels.
Moreover, the incident of gout in vegetarians, or mostly vegetarians, has always been significant and “much higher than is generally assumed.” (One mid-century estimate, for instance, put the incidence of gout in India among “largely vegetarians and teetotalers” at 7 %.)
Finally, there’s the repeated observation that eating more protein increases the excretion of uric acid from the kidney and, by doing so, decreases the level of uric acid in the blood.
This implies that the meat-gout hypothesis is at best debatable; the high protein content of meats should be beneficial, even if the purines are not.
By the 1990s, Gerald Reaven, among others, was reporting that insulin resistance and hyperinsulinemia raised uric acid levels, apparently by decreasing uric acid excretion by the kidney, just as they raised blood pressure by decreasing sodium excretion. “It appears that modulation of serum uric concentration by insulin resistance is exerted at the level of the kidney,” Reaven wrote, “the more insulin-resistant an individual, the higher the serum uric acid concentration.”
These observations would suggest that anything that raised insulin levels would in turn raise uric acid levels and might cause gout, which would implicate any high carbohydrate diet with sufficient calories.
Fructose, for instance, accelerates the breakdown of a molecule known as ATP, which is the primary source of energy for cellular reactions and is loaded with purines. (ATP stands for adenosine triphosphate; adenosine is a form of adenine, and adenine is a purine.) And so this in turn increases formation of uric acid.
Alcohol apparently raises uric acid levels through the same mechanism, although beer also has purines in it.
Fructose also stimulates the synthesis of purines directly, and the metabolism of fructose leads to the production of lactic acid, which in turn reduces the excretion of uric acid by the kidney and so raises uric acid concentrations indirectly by that mechanism while the glucose, though its effect on insulin, would also decrease uric acid excretion.
Thus, it would be reasonable to assume or at least to speculate that sugar is a likely cause of gout, and that the patterns of sugar consumption explain the appearance and distribution of the disease.
Some other factors may cause High Uric acid Concentration in bloods
- Kidney disease or kidney damage that prevents normal elimination of uric acid
- The increased breakdown of body cells that occurs with some types of cancer (including leukemia, lymphoma, and multiple myeloma) or cancer treatments, sickle cell anemia, hemolytic anemia, or heart failure.
- Certain disorders, such as preeclampsia, liver disease (cirrhosis), obesity, psoriasis, hypothyroidism, and low blood levels of parathyroid hormone.
- An inherited gene disorder called Lesch-Nyhan syndrome.
- Drugs, such as some diuretics, vitamin C, niacin, warfarin (such as coumadin), cyclosporine, levodopa, tacrolimus, and some medicines used to treat leukemia, lymphoma, or tuberculosis.
- Starvation causes the body to metabolize its own (purine-rich) tissues for energy.
- Exercise: Exercise may result in enhanced tissue breakdown and decreased renal excretion due to mild volume depletion.
- Lead intoxication
Some Myths About GOUT
Myth No. 1: Over time, gout will go away on its own.
Myth No. 2: Gout is a mild form of arthritis.
Myth No. 3: Gout is a rare condition.
Myth No. 4: Gout only affects the big toe.
Myth No. 5: A gout attack never lasts longer than 10 days.
Myth No. 6: Gout goes away between gout attacks.
Myth No. 7: Eating cherries can cure gout.
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